Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus

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Autor(es): dc.contributorInstituto Butantan-
Autor(es): dc.contributorUniversidade de São Paulo (USP)-
Autor(es): dc.contributorUniversidade do Estado de São Paulo-
Autor(es): dc.contributorWashington University in St. Louis-
Autor(es): dc.contributorMayo Clinic College of Medicine-
Autor(es): dc.contributorRutgers Cancer Institute of New Jersey-
Autor(es): dc.creatorCararo-Lopes, Eduardo-
Autor(es): dc.creatorDias, Matheus H.-
Autor(es): dc.creatorda Silva, Marcelo S.-
Autor(es): dc.creatorZeidler, Julianna D.-
Autor(es): dc.creatorVessoni, Alexandre T.-
Autor(es): dc.creatorReis, Marcelo S.-
Autor(es): dc.creatorBoccardo, Enrique-
Autor(es): dc.creatorArmelin, Hugo A.-
Data de aceite: dc.date.accessioned2025-08-21T16:32:58Z-
Data de disponibilização: dc.date.available2025-08-21T16:32:58Z-
Data de envio: dc.date.issued2022-04-29-
Data de envio: dc.date.issued2022-04-29-
Data de envio: dc.date.issued2021-01-31-
Fonte completa do material: dc.identifierhttp://dx.doi.org/10.1038/s41419-021-03476-3-
Fonte completa do material: dc.identifierhttp://hdl.handle.net/11449/231453-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/231453-
Descrição: dc.descriptionMalignant transformation involves an orchestrated rearrangement of cell cycle regulation mechanisms that must balance autonomic mitogenic impulses and deleterious oncogenic stress. Human papillomavirus (HPV) infection is highly prevalent in populations around the globe, whereas the incidence of cervical cancer is 0.15%. Since HPV infection primes cervical keratinocytes to undergo malignant transformation, we can assume that the balance between transforming mitogenic signals and oncogenic stress is rarely attained. We showed that highly transforming mitogenic signals triggered by HRasG12V activity in E6E7–HPV–keratinocytes generate strong replication and oxidative stresses. These stresses are counteracted by autophagy induction that buffers the rapid increase of ROS that is the main cause of genotoxic stress promoted by the oncoprotein. As a result, autophagy creates a narrow window of opportunity for malignant keratinocytes to emerge. This work shows that autophagy is crucial to allow the transition of E6E7 keratinocytes from an immortalized to a malignant state caused by HRasG12V.-
Descrição: dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)-
Descrição: dc.descriptionCenter of Toxins Immune-response and Cell Signaling Instituto Butantan-
Descrição: dc.descriptionDepartment of Biochemistry Instituto de Química Universidade de São Paulo-
Descrição: dc.descriptionDepartment of Chemical and Biological Sciences Instituto de Biociência Universidade do Estado de São Paulo-
Descrição: dc.descriptionDepartment of Medicine Washington University in St. Louis-
Descrição: dc.descriptionDepartment of Microbiology Instituto de Biociências Universidade de São Paulo-
Descrição: dc.descriptionKogod Aging Center Department of Anesthesiology and Perioperative Medicine Mayo Clinic College of Medicine-
Descrição: dc.descriptionRutgers Cancer Institute of New Jersey-
Idioma: dc.languageen-
Relação: dc.relationCell Death and Disease-
???dc.source???: dc.sourceScopus-
Título: dc.titleAutophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

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